Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (impress study)

Versaci, Francesco; Gaspardone, Achille; Tomai, Fabrizio; Russo, Paolo; Proietti, Igino; Ghini, Anna S.; Ribichini, Flavio; deFazio, Anna; Chiariello, Luigi; Gloffrè, Pier A.; Crea, Filippo

doi:10.1016/s0735-1097(02)80060-2

Cited by 18 publications

(24 citation statements)

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“…Therefore, an antiinflammatory treatment in patients after PCI with an extensive and prolonged inflammatory response might be of high clinical importance. In the IMPRESS Study for patients with persistant high CRP levels (> 5 mg/L) at 72 h after successful coronary stenting, oral prednisone therapy for 45 days was introduced and resulted in a noticeable reduction in clinical events and angiographic restenosis rate [22]. Bhatt suggested potential benefits of oral anti-proliferative agents, if validated in randomized clinical trails, to lower substantially the restenosis rate [17].…”

Section: Discussionmentioning

confidence: 99%

Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent restenosis – comparison with stable and unstable angina

et al. 2005

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Section: Discussionmentioning

confidence: 99%

Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent restenosis – comparison with stable and unstable angina

et al. 2005

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“…Thus, we observe in part CRP derived from atherosclerotic plaque in peripheral blood measurement [62]. CRP is also increased after PCI with the maximum increase at 48 h after the procedure, and the CRP at 72 h can predict restenosis [63].…”

Section: Inflammation In the Process Of Atherosclerosismentioning

confidence: 99%

Statin Therapy for Vascular Failure

Inoue

Node

2007

Cardiovasc Drugs Ther

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There is increasing evidence that statins reduce cardiovascular events such as coronary artery disease or stroke in hypercholesterolemic patients in both primary and secondary prevention. The striking benefit achieved with statin treatments in patients with a wide range of cholesterol levels cannot be attributed to their cholesterol lowering effect alone. Substantial data has recently accumulated showing that statins exert various effects on multiple targets, namely pleiotropic effects, especially targeting the concept of 'vascular failure', including the improvement of vascular endothelial function, inhibition of vascular smooth muscle cell proliferation and migration, anti-inflammatory actions, anti-oxidative effects or stabilization of vulnerable plaques. These effects have potential in the treatments of coronary artery disease in various settings, such as prevention of its onset as well as its progression, or plaque rupture. Statin therapy should be more extensively applied even in normolipidemic patients if there are additional risk factors such as hypertension, diabetes mellitus, or others. Furthermore, statins may be used to intervene in earlier stage risk conditions such as postprandial hyperlipidemia or hyperglycemia, insulin resistant state, masked hypertension, or metabolic syndrome to further reduce mortality or morbidity of coronary artery disease and heart failure.

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“…Consequently, inhibition of either the inflammatory response [126] or VSMC proliferation/migration [127] inhibits lesion development in a variety of models. Since glucocorticoids (dexamethasone) can inhibit inflammation and VSMC proliferation [121][122][123] and migration [128], it is not surprising that their potential as anti-atherosclerotic [129] and antirestenotic agents [130] has been investigated [6]. It is also possible, however, that the action of glucocorticoids on the vessel wall is deleterious in patients with vascular disease.…”

Section: Neointimal Proliferationmentioning

confidence: 99%

“…Dexamethasone reduces cholesterol ester accumulation in the aorta [133], and glucocorticoids (dexamethasone, hydrocortisone) inhibit neointimal lesion formation in rats [134,135], rabbits [136][137][138] and dogs [139] (with a few contradictory reports [140,141]). Clinical trials in humans, by contrast, have proved disappointing (with notable exceptions [130]): methylprednisolone did not inhibit restenosis after coronary angioplasty [142] or stent implantation [143], whilst the combination of a glucocor-570 P. W. F. Hadoke et al Intra-vascular glucocorticoid metabolism ticoid with colchicine increased the risk of coronary aneurysm following stent placement [144]. Discrepancies between clinical studies and animal models could be attributed to species differences or, more probably, to methodological variation (e.g.…”

Section: Neointimal Proliferationmentioning

confidence: 99%

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

Hadoke

Macdonald

Logie

et al. 2006

Cell. Mol. Life Sci.

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The ability of glucocorticoids to directly alter arterial function, structure and the inflammatory response to vascular injury may contribute to their well-established link with the development of cardiovascular disease. Recent studies have emphasised the importance of tissue-specific regulation of glucocorticoid availability by the 11 beta-hydroxysteroid dehydrogenase (11HSD) isozymes, which inter-convert active glucocorticoids and their inactive metabolites. The expression of both type 1 and type 2 11HSDs in the arterial wall suggests that prereceptor metabolism of glucocorticoids may have a direct impact on vascular physiology. Indeed there is evidence that 11HSDs influence glucocorticoid-mediated changes in vascular contractility, vascular structure, the inflammatory response to injury and the growth of new blood vessels. Hence, inhibition of 11HSD isozymes may provide a novel therapeutic target in vascular disease.

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Immunosuppressive therapy for the prevention of restenosis after coronary artery stent implantation (impress study)

Cited by 18 publications

References 0 publications

Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent restenosis – comparison with stable and unstable angina

Percutaneous coronary intervention triggers a systemic inflammatory response in patients treated for in-stent restenosis – comparison with stable and unstable angina

Statin Therapy for Vascular Failure

Intra-vascular glucocorticoid metabolism as a modulator of vascular structure and function

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